Inactivation of the wild-type p53 gene (TP53) by various genetic alterations is a major event in human tumorigenesis. More than 60% of human primary tumors exhibit a mutation in the p53 gene. Hematological malignancies present a rather low incidence of genetic alterations in this gene (10-20%). Nevertheless, epidemiological studies of the hematological malignancies indicate that the prognosis of patients with a mutation in the p53 gene is worse than those expressing the wild-type p53 protein. Correlations between drug resistance, altered apoptosis, and mutations in the p53 gene are found in hematological malignancies and leukemias. These issues, as well as the possibility of exploiting p53 and its various functions for new therapeutic strategies, are discussed in the present review.
Copyright 2003 Wiley-Liss, Inc.